To elucidate the role of PKG isoforms in transcriptional control of cyclin D1, we employed a series of expression vectors of PKG $1{alpha}$ and PKG $1{eta}$ which encode HA-tagged wild type and constitutively active (SD and ${Delta}N$) mutants. Our present study demonstrates that both the constitutively active mutants of PKG $1{eta}$ downregulate the transcription of cyclin D1 when transiently transfected in NIH3T3 cells, whereas PKG $1{alpha}$ mutants show weak inhibition. We further studied the transcriptional regulators of cyclin D1, such as, c-fos, NF-${kappa}B$, and CRE by using the luciferase reporter assay. Constitutively active mutants of PKG $1{eta}$ showed marked transcriptional downregulation of c-fos in NIH3T3 cells, whereas PKG $1{alpha}$ downregulated c-fos to a lesser extent. We also found that the constitutively active mutants of PKG negatively regulated the activation of NF-${kappa}B$ and CRE, suggesting their involvement in the regulation of cyclin D1.